During the next year we intend to continue our studies on genetic control of susceptibility to murine mammary tumor viruses (MuMTV) in mice. We are attempting to define the mechanisms by which the H-2 complex affects susceptibility in those examples already described. Since we have found that BALB.B and BALB/c mice differ in their responses to MuMTV(A), we are focusing on these two strains as an example of H-2 restriction. We have also broadened our studies to include the importance of non-H-2-linked genes in determining susceptibility to these viruses. For this purpose we are comparing the CXB recombinant inbred (RI) strains derived from BALB/c ByJ and C57BL ByJ strains for their susceptibility to MuMTV as judged by virus expression in the milk and by the development of mammary tumors. We are also examining the reactivity of T lymphocytes to MuMTV in a number of mouse strains which do not develop mammary tumors as well as syngeneic mice which carry milk-transmitted MuMTV and which do develop mammary tumors. This is being carried out using long-term cultures of specifically reactive T cells and T-cell hybrids. Finally, we are collaborating on a number of studies on the control of expression of endogenous MuMTV proviruses in a number of mouse strains. These studies will be extended to include the mechanisms for translational control of endogenous virus expression in C57BL mice, as well as the basis for the suppression of tumor development in crosses of C57BL mice with the C3Hf strain.